The Experts below are selected from a list of 15462 Experts worldwide ranked by ideXlab platform
Anita Jagota - One of the best experts on this subject based on the ideXlab platform.
-
Daily rhythms of serotonin metabolism and the expression of clock genes in suprachiasmatic nucleus of rotenone-induced Parkinson’s disease male Wistar rat model and effect of melatonin administration
Biogerontology, 2015Co-Authors: Ushodaya Mattam, Anita JagotaAbstract:The circadian system in suprachiasmatic nucleus (SCN) involves regulated serotonin levels and coordinated expression of various clock genes. To understand circadian disfunction in the Age-Related Neurodegenerative Disorder Parkinson’s disease (PD), the rotenone-induced PD (RIPD) male Wistar rat model was used. The alterations in the rhythmic dynamic equilibrium of interactions between the various components of serotonin metabolism and the molecular clock were measured. There was significant decrease in the mean 24 h levels of tryptophan, 5-hydroxytryptophan (5-HTP), serotonin (5-HT), N -acetyl serotonin (NAS) and melatonin (MEL) by approximately 63, 51, 76 and 96 % respectively ( p ≤ 0.05). However significant increase in 5-methoxy indole acetic acid (5-MIAA), 5-methoxy tryptophol (5-MTOH), 5-hydroxy tryptophol (5-HTOH) indicated increased serotonin catabolism with the abolition of daily rhythms of MEL, 5-HTP and 5-MIAA in RIPD. 24 h mean levels of rPer1 , rCry1 , rBmal1 reduced by about 0.5, 0.74 and 0.39-fold and increased for rPer2 by about 1.7-fold. The daily pulse of rPer2 , rCry1 , rCry2 and rBmal1 significantly decreased by 0.36, 0.6, 0.14, 0.1 and 0.2-fold. As melatonin, an antioxidant and an endogenous synchronizer of rhythm declined in RIPD male Wistar rat model, the effects of melatonin-administration on the rhythmic expression of various clock genes were studied. Interestingly, melatonin-administration resulted in restoration of the phase of rPer1 daily rhythm in RIPD indicating differential sensitivity of various clock components towards melatonin. The animals which were administered both rotenone and MEL for 48 days interestingly showed neuroprotective effects in dark phase on correlations between expression of various genes.
-
daily rhythms of serotonin metabolism and the expression of clock genes in suprachiasmatic nucleus of rotenone induced parkinson s disease male wistar rat model and effect of melatonin administration
Biogerontology, 2015Co-Authors: Ushodaya Mattam, Anita JagotaAbstract:The circadian system in suprachiasmatic nucleus (SCN) involves regulated serotonin levels and coordinated expression of various clock genes. To understand circadian disfunction in the Age-Related Neurodegenerative Disorder Parkinson’s disease (PD), the rotenone-induced PD (RIPD) male Wistar rat model was used. The alterations in the rhythmic dynamic equilibrium of interactions between the various components of serotonin metabolism and the molecular clock were measured. There was significant decrease in the mean 24 h levels of tryptophan, 5-hydroxytryptophan (5-HTP), serotonin (5-HT), N-acetyl serotonin (NAS) and melatonin (MEL) by approximately 63, 51, 76 and 96 % respectively (p ≤ 0.05). However significant increase in 5-methoxy indole acetic acid (5-MIAA), 5-methoxy tryptophol (5-MTOH), 5-hydroxy tryptophol (5-HTOH) indicated increased serotonin catabolism with the abolition of daily rhythms of MEL, 5-HTP and 5-MIAA in RIPD. 24 h mean levels of rPer1, rCry1, rBmal1 reduced by about 0.5, 0.74 and 0.39-fold and increased for rPer2 by about 1.7-fold. The daily pulse of rPer2, rCry1, rCry2 and rBmal1 significantly decreased by 0.36, 0.6, 0.14, 0.1 and 0.2-fold. As melatonin, an antioxidant and an endogenous synchronizer of rhythm declined in RIPD male Wistar rat model, the effects of melatonin-administration on the rhythmic expression of various clock genes were studied. Interestingly, melatonin-administration resulted in restoration of the phase of rPer1 daily rhythm in RIPD indicating differential sensitivity of various clock components towards melatonin. The animals which were administered both rotenone and MEL for 48 days interestingly showed neuroprotective effects in dark phase on correlations between expression of various genes.
Nihad Abdel-monem - One of the best experts on this subject based on the ideXlab platform.
-
Neuroprotective effect of ipriflavone against scopolamine-induced memory impairment in rats
Psychopharmacology, 2017Co-Authors: Hani S. Hafez, Doaa A. Ghareeb, Samar R. Saleh, Mariam M. Abady, Maha A. El Demellawy, Hend Hussien, Nihad Abdel-monemAbstract:Background Alzheimer’s disease is an Age-Related Neurodegenerative Disorder characterized clinically by a progressive loss of memory and cognitive functions resulting in severe dementia. Ipriflavone (IPRI) is a non-hormonal, semi-synthetic isoflavone, clinically used in some countries for the treatment and prevention of postmenopausal osteoporosis. Moreover, ipriflavone is a non-peptidomimetic small molecule AChE inhibitor with an improved bioavailability after systemic administration, due to its efficient blood-brain barrier permeability in comparison with peptidomimetic inhibitors. Objective The present study aimed to evaluate the possible enhancing effects of IPRI on memory impairments caused by scopolamine administration. Methods Male rats were administered IPRI (50 mg/kg, oral) 2 h before scopolamine injection (2 mg/kg, intraperitoneally injected) daily for 4 weeks. Effects of IPRI on acetylcholinesterase activity, amyloid-β precursor processing, and neuroplasticity in the rats’ hippocampus were investigated. Results Daily administration of IPRI reverted memory impairment caused by scopolamine as measured by the reduction of the escape latency. IPRI significantly alleviated the oxidative stress and restored the mRNA expression of both cAMP-response element-binding protein and brain-derived neurotrophic factor in the hippocampus. Furthermore, it significantly increased the expression of ADAM10 and ADAM17 (two putative α-secretase enzymes) and phosphorylated extracellular signal-regulated kinase 1/2 (pERK1/2) that associated with decreased expression of β-secretase (BACE) in the hippocampus. Finally, both the amyloid-β (Aβ) and Tau pathologies were reduced. Conclusions IPRI showed promising neuroprotective effects against scopolamine-induced memory dysfunction in rats. These findings contributed to the stimulation of α-secretase enzymes, the activation of MAPK/ERK1/2, and the alleviation of oxidative stress.
-
Neuroprotective effect of ipriflavone against scopolamine-induced memory impairment in rats.
Psychopharmacology, 2017Co-Authors: Hani S. Hafez, Doaa A. Ghareeb, Samar R. Saleh, Mariam M. Abady, Maha A. El Demellawy, Hend M. Hussien, Nihad Abdel-monemAbstract:Background Alzheimer’s disease is an Age-Related Neurodegenerative Disorder characterized clinically by a progressive loss of memory and cognitive functions resulting in severe dementia. Ipriflavone (IPRI) is a non-hormonal, semi-synthetic isoflavone, clinically used in some countries for the treatment and prevention of postmenopausal osteoporosis. Moreover, ipriflavone is a non-peptidomimetic small molecule AChE inhibitor with an improved bioavailability after systemic administration, due to its efficient blood-brain barrier permeability in comparison with peptidomimetic inhibitors.
Ushodaya Mattam - One of the best experts on this subject based on the ideXlab platform.
-
Daily rhythms of serotonin metabolism and the expression of clock genes in suprachiasmatic nucleus of rotenone-induced Parkinson’s disease male Wistar rat model and effect of melatonin administration
Biogerontology, 2015Co-Authors: Ushodaya Mattam, Anita JagotaAbstract:The circadian system in suprachiasmatic nucleus (SCN) involves regulated serotonin levels and coordinated expression of various clock genes. To understand circadian disfunction in the Age-Related Neurodegenerative Disorder Parkinson’s disease (PD), the rotenone-induced PD (RIPD) male Wistar rat model was used. The alterations in the rhythmic dynamic equilibrium of interactions between the various components of serotonin metabolism and the molecular clock were measured. There was significant decrease in the mean 24 h levels of tryptophan, 5-hydroxytryptophan (5-HTP), serotonin (5-HT), N -acetyl serotonin (NAS) and melatonin (MEL) by approximately 63, 51, 76 and 96 % respectively ( p ≤ 0.05). However significant increase in 5-methoxy indole acetic acid (5-MIAA), 5-methoxy tryptophol (5-MTOH), 5-hydroxy tryptophol (5-HTOH) indicated increased serotonin catabolism with the abolition of daily rhythms of MEL, 5-HTP and 5-MIAA in RIPD. 24 h mean levels of rPer1 , rCry1 , rBmal1 reduced by about 0.5, 0.74 and 0.39-fold and increased for rPer2 by about 1.7-fold. The daily pulse of rPer2 , rCry1 , rCry2 and rBmal1 significantly decreased by 0.36, 0.6, 0.14, 0.1 and 0.2-fold. As melatonin, an antioxidant and an endogenous synchronizer of rhythm declined in RIPD male Wistar rat model, the effects of melatonin-administration on the rhythmic expression of various clock genes were studied. Interestingly, melatonin-administration resulted in restoration of the phase of rPer1 daily rhythm in RIPD indicating differential sensitivity of various clock components towards melatonin. The animals which were administered both rotenone and MEL for 48 days interestingly showed neuroprotective effects in dark phase on correlations between expression of various genes.
-
daily rhythms of serotonin metabolism and the expression of clock genes in suprachiasmatic nucleus of rotenone induced parkinson s disease male wistar rat model and effect of melatonin administration
Biogerontology, 2015Co-Authors: Ushodaya Mattam, Anita JagotaAbstract:The circadian system in suprachiasmatic nucleus (SCN) involves regulated serotonin levels and coordinated expression of various clock genes. To understand circadian disfunction in the Age-Related Neurodegenerative Disorder Parkinson’s disease (PD), the rotenone-induced PD (RIPD) male Wistar rat model was used. The alterations in the rhythmic dynamic equilibrium of interactions between the various components of serotonin metabolism and the molecular clock were measured. There was significant decrease in the mean 24 h levels of tryptophan, 5-hydroxytryptophan (5-HTP), serotonin (5-HT), N-acetyl serotonin (NAS) and melatonin (MEL) by approximately 63, 51, 76 and 96 % respectively (p ≤ 0.05). However significant increase in 5-methoxy indole acetic acid (5-MIAA), 5-methoxy tryptophol (5-MTOH), 5-hydroxy tryptophol (5-HTOH) indicated increased serotonin catabolism with the abolition of daily rhythms of MEL, 5-HTP and 5-MIAA in RIPD. 24 h mean levels of rPer1, rCry1, rBmal1 reduced by about 0.5, 0.74 and 0.39-fold and increased for rPer2 by about 1.7-fold. The daily pulse of rPer2, rCry1, rCry2 and rBmal1 significantly decreased by 0.36, 0.6, 0.14, 0.1 and 0.2-fold. As melatonin, an antioxidant and an endogenous synchronizer of rhythm declined in RIPD male Wistar rat model, the effects of melatonin-administration on the rhythmic expression of various clock genes were studied. Interestingly, melatonin-administration resulted in restoration of the phase of rPer1 daily rhythm in RIPD indicating differential sensitivity of various clock components towards melatonin. The animals which were administered both rotenone and MEL for 48 days interestingly showed neuroprotective effects in dark phase on correlations between expression of various genes.
Peter Davies - One of the best experts on this subject based on the ideXlab platform.
-
amp activated protein kinase signaling activation by resveratrol modulates amyloid β peptide metabolism
Journal of Biological Chemistry, 2010Co-Authors: Valerie Vingtdeux, Luca Giliberto, Pallavi Chandakkar, Jessica Lobo, Elsa M. Janle, Haitian Zhao, Qingli Wu, Mario G. Ferruzzi, James E Simon, Peter DaviesAbstract:Alzheimer disease is an Age-Related Neurodegenerative Disorder characterized by amyloid-β (Aβ) peptide deposition into cerebral amyloid plaques. The natural polyphenol resveratrol promotes anti-aging pathways via the activation of several metabolic sensors, including the AMP-activated protein kinase (AMPK). Resveratrol also lowers Aβ levels in cell lines; however, the underlying mechanism responsible for this effect is largely unknown. Moreover, the bioavailability of resveratrol in the brain remains uncertain. Here we show that AMPK signaling controls Aβ metabolism and mediates the anti-amyloidogenic effect of resveratrol in non-neuronal and neuronal cells, including in mouse primary neurons. Resveratrol increased cytosolic calcium levels and promoted AMPK activation by the calcium/calmodulin-dependent protein kinase kinase-β. Direct pharmacological and genetic activation of AMPK lowered extracellular Aβ accumulation, whereas AMPK inhibition reduced the effect of resveratrol on Aβ levels. Furthermore, resveratrol inhibited the AMPK target mTOR (mammalian target of rapamycin) to trigger autophagy and lysosomal degradation of Aβ. Finally, orally administered resveratrol in mice was detected in the brain where it activated AMPK and reduced cerebral Aβ levels and deposition in the cortex. These data suggest that resveratrol and pharmacological activation of AMPK have therapeutic potential against Alzheimer disease.
-
amp activated protein kinase signaling activation by resveratrol modulates amyloid β peptide metabolism
Journal of Biological Chemistry, 2010Co-Authors: Valerie Vingtdeux, Luca Giliberto, Pallavi Chandakkar, Jessica Lobo, Elsa M. Janle, Haitian Zhao, Mario G. Ferruzzi, Peter Davies, James E Simon, Philippe MarambaudAbstract:Alzheimer disease is an Age-Related Neurodegenerative Disorder characterized by amyloid-beta (Abeta) peptide deposition into cerebral amyloid plaques. The natural polyphenol resveratrol promotes anti-aging pathways via the activation of several metabolic sensors, including the AMP-activated protein kinase (AMPK). Resveratrol also lowers Abeta levels in cell lines; however, the underlying mechanism responsible for this effect is largely unknown. Moreover, the bioavailability of resveratrol in the brain remains uncertain. Here we show that AMPK signaling controls Abeta metabolism and mediates the anti-amyloidogenic effect of resveratrol in non-neuronal and neuronal cells, including in mouse primary neurons. Resveratrol increased cytosolic calcium levels and promoted AMPK activation by the calcium/calmodulin-dependent protein kinase kinase-beta. Direct pharmacological and genetic activation of AMPK lowered extracellular Abeta accumulation, whereas AMPK inhibition reduced the effect of resveratrol on Abeta levels. Furthermore, resveratrol inhibited the AMPK target mTOR (mammalian target of rapamycin) to trigger autophagy and lysosomal degradation of Abeta. Finally, orally administered resveratrol in mice was detected in the brain where it activated AMPK and reduced cerebral Abeta levels and deposition in the cortex. These data suggest that resveratrol and pharmacological activation of AMPK have therapeutic potential against Alzheimer disease.
Hani S. Hafez - One of the best experts on this subject based on the ideXlab platform.
-
Neuroprotective effect of ipriflavone against scopolamine-induced memory impairment in rats
Psychopharmacology, 2017Co-Authors: Hani S. Hafez, Doaa A. Ghareeb, Samar R. Saleh, Mariam M. Abady, Maha A. El Demellawy, Hend Hussien, Nihad Abdel-monemAbstract:Background Alzheimer’s disease is an Age-Related Neurodegenerative Disorder characterized clinically by a progressive loss of memory and cognitive functions resulting in severe dementia. Ipriflavone (IPRI) is a non-hormonal, semi-synthetic isoflavone, clinically used in some countries for the treatment and prevention of postmenopausal osteoporosis. Moreover, ipriflavone is a non-peptidomimetic small molecule AChE inhibitor with an improved bioavailability after systemic administration, due to its efficient blood-brain barrier permeability in comparison with peptidomimetic inhibitors. Objective The present study aimed to evaluate the possible enhancing effects of IPRI on memory impairments caused by scopolamine administration. Methods Male rats were administered IPRI (50 mg/kg, oral) 2 h before scopolamine injection (2 mg/kg, intraperitoneally injected) daily for 4 weeks. Effects of IPRI on acetylcholinesterase activity, amyloid-β precursor processing, and neuroplasticity in the rats’ hippocampus were investigated. Results Daily administration of IPRI reverted memory impairment caused by scopolamine as measured by the reduction of the escape latency. IPRI significantly alleviated the oxidative stress and restored the mRNA expression of both cAMP-response element-binding protein and brain-derived neurotrophic factor in the hippocampus. Furthermore, it significantly increased the expression of ADAM10 and ADAM17 (two putative α-secretase enzymes) and phosphorylated extracellular signal-regulated kinase 1/2 (pERK1/2) that associated with decreased expression of β-secretase (BACE) in the hippocampus. Finally, both the amyloid-β (Aβ) and Tau pathologies were reduced. Conclusions IPRI showed promising neuroprotective effects against scopolamine-induced memory dysfunction in rats. These findings contributed to the stimulation of α-secretase enzymes, the activation of MAPK/ERK1/2, and the alleviation of oxidative stress.
-
Neuroprotective effect of ipriflavone against scopolamine-induced memory impairment in rats.
Psychopharmacology, 2017Co-Authors: Hani S. Hafez, Doaa A. Ghareeb, Samar R. Saleh, Mariam M. Abady, Maha A. El Demellawy, Hend M. Hussien, Nihad Abdel-monemAbstract:Background Alzheimer’s disease is an Age-Related Neurodegenerative Disorder characterized clinically by a progressive loss of memory and cognitive functions resulting in severe dementia. Ipriflavone (IPRI) is a non-hormonal, semi-synthetic isoflavone, clinically used in some countries for the treatment and prevention of postmenopausal osteoporosis. Moreover, ipriflavone is a non-peptidomimetic small molecule AChE inhibitor with an improved bioavailability after systemic administration, due to its efficient blood-brain barrier permeability in comparison with peptidomimetic inhibitors.
